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Journal articles on the topic 'Eklf'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Hodge, Denise, Elise Coghill, Janelle Keys, Tina Maguire, Belinda Hartmann, Alasdair McDowall, Mitchell Weiss, Sean Grimmond, and Andrew Perkins. "A global role for EKLF in definitive and primitive erythropoiesis." Blood 107, no. 8 (April 15, 2006): 3359–70. http://dx.doi.org/10.1182/blood-2005-07-2888.

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Abstract Erythroid Kruppel-like factor (EKLF, KLF1) plays an important role in definitive erythropoiesis and β-globin gene regulation but failure to rectify lethal fetal anemia upon correction of globin chain imbalance suggested additional critical EKLF target genes. We employed expression profiling of EKLF-null fetal liver and EKLF-null erythroid cell lines containing an inducible EKLF-estrogen receptor (EKLF-ER) fusion construct to search for such targets. An overlapping list of EKLF-regulated genes from the 2 systems included α-hemoglobin stabilizing protein (AHSP), cytoskeletal proteins, h

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2

Pilon, Andre M., Douglas G. Nilson, Dewang Zhou, Jose Sangerman, Tim M. Townes, David M. Bodine, and Patrick G. Gallagher. "Alterations in Expression and Chromatin Configuration of the Alpha Hemoglobin-Stabilizing Protein Gene in Erythroid Krüppel-Like Factor-Deficient Mice." Molecular and Cellular Biology 26, no. 11 (June 1, 2006): 4368–77. http://dx.doi.org/10.1128/mcb.02216-05.

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ABSTRACT Erythroid Krüppel-like factor (EKLF) is an erythroid zinc finger protein identified by its interaction with a CACCC sequence in the β-globin promoter, where it establishes local chromatin structure permitting β-globin gene transcription. We sought to identify other EKLF target genes and determine the chromatin status of these genes in the presence and absence of EKLF. We identified alpha hemoglobin-stabilizing protein (AHSP) by subtractive hybridization and demonstrated a 95 to 99.9% reduction in AHSP mRNA and the absence of AHSP in EKLF-deficient cells. Chromatin at the AHSP promote

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3

Basu, Priyadarshi, Tina K. Lung, Wafaa Lemsaddek, Thanh Giang Sargent, David C. Williams, Mohua Basu, Latasha C. Redmond, Jerry B. Lingrel, Jack L. Haar та Joyce A. Lloyd. "EKLF and KLF2 have compensatory roles in embryonic β-globin gene expression and primitive erythropoiesis". Blood 110, № 9 (1 листопада 2007): 3417–25. http://dx.doi.org/10.1182/blood-2006-11-057307.

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Abstract The Krüppel-like C2/H2 zinc finger transcription factors (KLFs) control development and differentiation. Erythroid Krüppel-like factor (EKLF or KLF1) regulates adult β-globin gene expression and is necessary for normal definitive erythropoiesis. KLF2 is required for normal embryonic Ey- and βh1-, but not adult βglobin, gene expression in mice. Both EKLF and KLF2 play roles in primitive erythroid cell development. To investigate potential interactions between these genes, EKLF/KLF2 double-mutant embryos were analyzed. EKLF−/−KLF2−/− mice appear anemic at embryonic day 10.5 (E10.5) and

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4

Pilon, Andre M., Murat O. Arcasoy, Holly K. Dressman, Serena E. Vayda, Yelena D. Maksimova, Jose I. Sangerman, Patrick G. Gallagher, and David M. Bodine. "Failure of Terminal Erythroid Differentiation in EKLF-Deficient Mice Is Associated with Cell Cycle Perturbation and Reduced Expression of E2F2." Molecular and Cellular Biology 28, no. 24 (October 13, 2008): 7394–401. http://dx.doi.org/10.1128/mcb.01087-08.

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ABSTRACT Erythroid Krüppel-like factor (EKLF) is a Krüppel-like transcription factor identified as a transcriptional activator and chromatin modifier in erythroid cells. EKLF-deficient (Eklf −/− ) mice die at day 14.5 of gestation from severe anemia. In this study, we demonstrate that early progenitor cells fail to undergo terminal erythroid differentiation in Eklf −/− embryos. To discover potential EKLF target genes responsible for the failure of erythropoiesis, transcriptional profiling was performed with RNA from wild-type and Eklf −/− early erythroid progenitor cells. These analyses iden

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5

Pilon, Andre M., Subramanian S. Ajay, Swathi Ashok Kumar, Laurie A. Steiner, Praveen F. Cherukuri, Stephen Wincovitch, Stacie M. Anderson, et al. "Genome-wide ChIP-Seq reveals a dramatic shift in the binding of the transcription factor erythroid Kruppel-like factor during erythrocyte differentiation." Blood 118, no. 17 (October 27, 2011): e139-e148. http://dx.doi.org/10.1182/blood-2011-05-355107.

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Abstract Erythropoiesis is dependent on the activity of transcription factors, including the erythroid-specific erythroid Kruppel-like factor (EKLF). ChIP followed by massively parallel sequencing (ChIP-Seq) is a powerful, unbiased method to map trans-factor occupancy. We used ChIP-Seq to study the interactome of EKLF in mouse erythroid progenitor cells and more differentiated erythroblasts. We correlated these results with the nuclear distribution of EKLF, RNA-Seq analysis of the transcriptome, and the occupancy of other erythroid transcription factors. In progenitor cells, EKLF is found pred

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6

Perkins, Andrew C., Elise Coghill, Tina Maguire, Belinda Hartmann, Alasdair McDowall, Mitchell Weiss, Sean Grimmond, Janelle Keys, and Denise Hodge. "A Global Role for EKLF in Definitive and Primitive Erythropoiesis." Blood 106, no. 11 (November 16, 2005): 1745. http://dx.doi.org/10.1182/blood.v106.11.1745.1745.

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Abstract Erythroid Kruppel-like factor (EKLF or Klf1) is an erythroid specific C2H2 zinc-finger transcription factor which is essential for definitive erythropoiesis and β-globin gene expression. The absence of EKLF results in fatal anaemia but correction of globin chain imbalance does result in rescue, suggesting the existence of additional EKLF target genes. The aim of this study was to search for such genes by expression profiling. We performed profiling on fetal livers from wild-type versus EKLF null litter mates, and also EKLF null erythroid cell lines containing an inducible EKLF-ERTM fu

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7

Coghill, Elise, Sarah Eccleston, Vanessa Fox, Loretta Cerruti, Clark Brown, John Cunningham, Stephen Jane, and Andrew Perkins. "Erythroid Kruppel-like factor (EKLF) coordinates erythroid cell proliferation and hemoglobinization in cell lines derived from EKLF null mice." Blood 97, no. 6 (March 15, 2001): 1861–68. http://dx.doi.org/10.1182/blood.v97.6.1861.

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Erythroid Kruppel-like factor (EKLF) is a transcription factor of the C2H2 zinc-finger class that is essential for definitive erythropoiesis. We generated immortal erythroid cell lines from EKLF−/− fetal liver progenitor cells that harbor a single copy of the entire human β-globin locus and then reintroduced EKLF as a tamoxifen-inducible, EKLF–mutant estrogen receptor (EKLF-ER™) fusion protein. Addition of tamoxifen resulted in enhanced differentiation and hemoglobinization, coupled with reduced proliferation. Human β-globin gene expression increased significantly, whereas γ-globin transcripts

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8

Pilon, Andre M., Elliott H. Margulies, Hatice Ozel Abaan, Amy Werner Allen, Tim M. Townes, Abbie M. Frederick, Dewang Zhou, Patrick G. Gallagher, and David M. Bodine. "Genome-Wide Analysis of EKLF Occupancy in Erythroid Chromatin Reveals 5′, 3′ and Intragenic Binding Sites in EKLF Target Genes." Blood 112, no. 11 (November 16, 2008): 283. http://dx.doi.org/10.1182/blood.v112.11.283.283.

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Abstract Erythroid Kruppel-Like Factor (EKLF; KLF1) is the founding member of the Kruppel family of transcription factors, with 3 C2H2 zinc-fingers that bind a 9-base consensus sequence (NCNCNCCCN). The functions of EKLF, first identified as an activator of the beta-globin locus, include gene activation and chromatin remodeling. Our knowledge of genes regulated by EKLF is limited, as EKLF-deficient mice die by embryonic day 15 (E15), due to a severe anemia. Analysis of E13.5 wild type and EKLF-deficient fetal liver (FL) erythroid cells revealed that EKLF-deficient cells fail to complete termin

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9

Perkins, Andrew C., Janelle R. Keys, Denise J. Hodge, and Michael R. Tallack. "Erythroid Kruppel-Like Factor Regulates E2F4 and the G1 Cdk Inhibitor, p18." Blood 106, no. 11 (November 16, 2005): 1357. http://dx.doi.org/10.1182/blood.v106.11.1357.1357.

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Abstract Erythroid Kruppel-Like Factor (EKLF) is a zinc finger transcription factor which is essential for β-globin gene expression. Knockout mice die from anemia at E15, but restoration of globin chain imbalance does not rescue anemia or increase survival. Cell lines derived from EKLF null mice undergo proliferation arrest upon reactivation of a conditional EKLF-ER fusion protein, suggesting a role in cell cycle control. A transcriptional profiling experiment comparing the global gene expression in EKLF null and wild type fetal liver identified many differentially expressed genes, a number of

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10

Drissen, Roy, Marieke von Lindern, Andrea Kolbus, Siska Driegen, Peter Steinlein, Hartmut Beug, Frank Grosveld, and Sjaak Philipsen. "The Erythroid Phenotype of EKLF-Null Mice: Defects in Hemoglobin Metabolism and Membrane Stability." Molecular and Cellular Biology 25, no. 12 (June 15, 2005): 5205–14. http://dx.doi.org/10.1128/mcb.25.12.5205-5214.2005.

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ABSTRACT Development of red blood cells requires the correct regulation of cellular processes including changes in cell morphology, globin expression and heme synthesis. Transcription factors such as erythroid Krüppel-like factor EKLF (Klf1) play a critical role in erythropoiesis. Mice lacking EKLF die around embryonic day 14 because of defective definitive erythropoiesis, partly caused by a deficit in β-globin expression. To identify additional target genes, we analyzed the phenotype and gene expression profiles of wild-type and EKLF null primary erythroid progenitors that were differentiate

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11

Asano, Haruhiko, та George Stamatoyannopoulos. "Activation of β-Globin Promoter by Erythroid Krüppel-Like Factor". Molecular and Cellular Biology 18, № 1 (1 січня 1998): 102–9. http://dx.doi.org/10.1128/mcb.18.1.102.

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ABSTRACT Erythroid Krüppel-like factor (EKLF), an erythroid tissue-specific Krüppel-type zinc finger protein, binds to the β-globin gene CACCC box and is essential for β-globin gene expression. EKLF does not activate the γ gene, the CACCC sequence of which differs from that of the β gene. To test whether the CACCC box sequence difference is the primary determinant of the selective activation of the β gene by EKLF, the CACCC boxes of β and γ genes were swapped and the resulting promoter activities were assayed by transient transfections in CV-1 cells. EKLF activated the β promoter carrying a

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12

Jansen, Valerie M., Shaji Ramachandran, Aurelie Desgardin, Jin He, Vishwas Parekh, Stephen M. Jane та John M. Cunningham. "Context-Specific Roles for Erythroid Krüppel-Like Factor (EKLF) in Co-Ordinate High Level Expression of the Murine α- and β-Globin Genes." Blood 108, № 11 (16 листопада 2006): 365. http://dx.doi.org/10.1182/blood.v108.11.365.365.

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Abstract Binding of EKLF to the proximal promoter CACC motif is essential for high-level tissue-specific β-globin gene expression. More recent studies have demonstrated that EKLF regulates expression of other erythroid-specific genes, suggesting a broad role for EKLF in co-ordinating gene transcription in differentiating erythroblasts. Given these observations, we hypothesized that EKLF may play a role in synchronizing α- and β-globin gene expression. Supporting this model, studies of fetal erythroblasts derived from EKLF-null embryos revealed a 3-fold reduction in murine α-globin gene express

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13

Steiner, Laurie A., Vincent P. Schulz, Yelena Maksimova, Milind Mahajan, David M. Bodine, and Patrick G. Gallagher. "Dynamic CO-Localization of GATA1, NFE2, and EKLF and Changes in Gene Expression During Hematopoiesis." Blood 116, no. 21 (November 19, 2010): 741. http://dx.doi.org/10.1182/blood.v116.21.741.741.

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Abstract Abstract 741 Regulation of lineage choice during the development and differentiation of erythroid cells in hematopoiesis is a complex process. GATA1, NFE2, and EKLF are transcription factors critical for erythropoiesis. Focused studies, including detailed analyses of the human beta globin gene locus and a select group of erythrocyte membrane protein genes, have revealed that these three transcription factors may co-localize at common regulatory sites in erythroid-expressed genes. To address the hypothesis that GATA1, NFE2, and EKLF frequently co-localize on critical regulatory element

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14

Perkins, A. C., K. R. Peterson, G. Stamatoyannopoulos, H. E. Witkowska та S. H. Orkin. "Fetal expression of a human Aγ globin transgene rescues globin chain imbalance but not hemolysis in EKLF null mouse embryos". Blood 95, № 5 (1 березня 2000): 1827–33. http://dx.doi.org/10.1182/blood.v95.5.1827.004k10_1827_1833.

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Mice lacking the erythroid Kruppel-like factor (EKLF) die in utero at embryonic day 15 (E15) from severe anemia. EKLF−/− embryos display a marked deficit in β-globin gene expression. To test whether β-globin deficiency was solely responsible for the anemia and intrauterine death, we corrected the globin chain imbalance in EKLF−/− embryos by breeding with a strain of mice that express high levels of human γ-globin. Despite efficient production of hybrid m2-hγ2 hemoglobin in the fetal livers of EKLF−/− animals, hemolysis was not corrected and survival was not prolonged. We concluded that defici

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15

Hung, Chun-Hao, Keh-Yang Wang, Yae-Huei Liou, Jing-Ping Wang, Anna Yu-Szu Huang, Tung-Liang Lee, Si-Tse Jiang, Nah-Shih Liao, Yu-Chiau Shyu, and Che-Kun James Shen. "Negative Regulation of the Differentiation of Flk2− CD34− LSK Hematopoietic Stem Cells by EKLF/KLF1." International Journal of Molecular Sciences 21, no. 22 (November 10, 2020): 8448. http://dx.doi.org/10.3390/ijms21228448.

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Erythroid Krüppel-like factor (EKLF/KLF1) was identified initially as a critical erythroid-specific transcription factor and was later found to be also expressed in other types of hematopoietic cells, including megakaryocytes and several progenitors. In this study, we have examined the regulatory effects of EKLF on hematopoiesis by comparative analysis of E14.5 fetal livers from wild-type and Eklf gene knockout (KO) mouse embryos. Depletion of EKLF expression greatly changes the populations of different types of hematopoietic cells, including, unexpectedly, the long-term hematopoietic stem cel

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16

Gregory, RC, DJ Taxman, D. Seshasayee, MH Kensinger, JJ Bieker, and DM Wojchowski. "Functional interaction of GATA1 with erythroid Kruppel-like factor and Sp1 at defined erythroid promoters." Blood 87, no. 5 (March 1, 1996): 1793–801. http://dx.doi.org/10.1182/blood.v87.5.1793.1793.

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Abstract GATA and CACC elements commonly are codistributed within the regulatory domains of a variety of erythroid genes. Using Drosophila S2 cells, the actions of GATA1, Sp1, and erythroid Kruppel-like factor (EKLF) at these elements within model erythroid promoters have been assessed. For each promoter studied (erythroid pyruvate kinase, glycophorin B, and a murine betamaj globin-derived construct, GCT) Sp1 and EKLF each activated transcription despite differences in CACC element sequence, orientation, and positioning. However, GATA1 acted in apparent cooperativity with Sp1 at the pyruvate k

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Gregory, RC, DJ Taxman, D. Seshasayee, MH Kensinger, JJ Bieker, and DM Wojchowski. "Functional interaction of GATA1 with erythroid Kruppel-like factor and Sp1 at defined erythroid promoters." Blood 87, no. 5 (March 1, 1996): 1793–801. http://dx.doi.org/10.1182/blood.v87.5.1793.bloodjournal8751793.

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GATA and CACC elements commonly are codistributed within the regulatory domains of a variety of erythroid genes. Using Drosophila S2 cells, the actions of GATA1, Sp1, and erythroid Kruppel-like factor (EKLF) at these elements within model erythroid promoters have been assessed. For each promoter studied (erythroid pyruvate kinase, glycophorin B, and a murine betamaj globin-derived construct, GCT) Sp1 and EKLF each activated transcription despite differences in CACC element sequence, orientation, and positioning. However, GATA1 acted in apparent cooperativity with Sp1 at the pyruvate kinase pro

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18

Sengupta, Tanushri, Ken Chen, Eric Milot та James J. Bieker. "Acetylation of EKLF Is Essential for Epigenetic Modification and Transcriptional Activation of the β-Globin Locus". Molecular and Cellular Biology 28, № 20 (18 серпня 2008): 6160–70. http://dx.doi.org/10.1128/mcb.00919-08.

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ABSTRACT Posttranslational modifications of transcription factors provide alternate protein interaction platforms that lead to varied downstream effects. We have investigated how the acetylation of EKLF plays a role in its ability to alter the β-like globin locus chromatin structure and activate transcription of the adult β-globin gene. By establishing an EKLF-null erythroid line whose closed β-locus chromatin structure and silent β-globin gene status can be rescued by retroviral infection of EKLF, we demonstrate the importance of EKLF acetylation at lysine 288 in the recruitment of CBP to the

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19

Miller, I. J., and J. J. Bieker. "A novel, erythroid cell-specific murine transcription factor that binds to the CACCC element and is related to the Krüppel family of nuclear proteins." Molecular and Cellular Biology 13, no. 5 (May 1993): 2776–86. http://dx.doi.org/10.1128/mcb.13.5.2776-2786.1993.

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We describe a novel erythroid cell-specific cDNA (EKLF [erythroid Krüppel-like factor]) isolated by enriching for genes expressed in a mouse erythroleukemia cell line but not expressed in a mouse monocyte-macrophage cell line. The complete cDNA sequence is predicted to encode a protein of approximately 38,000 Da that contains a proline-rich amino domain and three TFIIIA-like zinc fingers within the carboxy domain. Additional sequence analyses reveal that the EKLF zinc fingers are most homologous to the Krüppel family of transcription factors and also allow us to predict potential DNA-binding t

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20

Miller, I. J., and J. J. Bieker. "A novel, erythroid cell-specific murine transcription factor that binds to the CACCC element and is related to the Krüppel family of nuclear proteins." Molecular and Cellular Biology 13, no. 5 (May 1993): 2776–86. http://dx.doi.org/10.1128/mcb.13.5.2776.

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We describe a novel erythroid cell-specific cDNA (EKLF [erythroid Krüppel-like factor]) isolated by enriching for genes expressed in a mouse erythroleukemia cell line but not expressed in a mouse monocyte-macrophage cell line. The complete cDNA sequence is predicted to encode a protein of approximately 38,000 Da that contains a proline-rich amino domain and three TFIIIA-like zinc fingers within the carboxy domain. Additional sequence analyses reveal that the EKLF zinc fingers are most homologous to the Krüppel family of transcription factors and also allow us to predict potential DNA-binding t

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21

Mukherjee, Kaustav, James J. Bieker, and Venkata Srinivas Mohan Nimai Dangeti. "EKLF/Klf1 Regulates Erythroid Transcription By Its Pioneering Activity and Subsequent Control of RNA Pol II Pause-Release." Blood 138, Supplement 1 (November 5, 2021): 283. http://dx.doi.org/10.1182/blood-2021-151470.

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Abstract EKLF/Klf1 is a master transcriptional activator of critical genes that regulate both erythroid fate specification and terminal erythroid maturation. EKLF binds to DNA using three Zn-fingers at its C-terminus while the N-terminus constitutes a transcription activation domain (TAD) that interacts with various transcription co-factors including the protein acetylase CBP. An autosomal semi-dominant mutation at a single residue (E339D) in the mouse EKLF Zn-finger leads to Neonatal anemia (Nan). A mutation at the same residue in human EKLF (E325K) causes Congenital Dyserythropoietic Anemia

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Pilon, Andre M., Subramanian S. Ajay, Hatice Ozel Abaan, Elliott H. Margulies, Patrick G. Gallagher, and David M. Bodine. "Genome-Wide ChIP-Seq Reveals a Dramatic Shift in the EKLF Binding Profile Between Erythroid Progenitors and Erythroblasts." Blood 114, no. 22 (November 20, 2009): 565. http://dx.doi.org/10.1182/blood.v114.22.565.565.

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Abstract Abstract 565 Erythroid Kruppel-Like Factor (EKLF; KLF1) is the founding member of the Kruppel family of C2H2 zinc finger transcription factors. First identified as an activator of the beta-globin locus, EKLF facilitates chromatin remodeling and transcriptional activation of target genes, at least in part through recognition of a 9-base consensus motif (NCNCNCCCN). By comparing the transcriptional profiles of E13.5 wild type and Eklf-/- mice, we demonstrated that the lethal failure to complete definitive erythropoiesis in the fetal liver (FL) was due in part to dysregulation of an EKLF

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23

Zhang, Wenjun, Shilpa Kadam, Beverly M. Emerson, and James J. Bieker. "Site-Specific Acetylation by p300 or CREB Binding Protein Regulates Erythroid Krüppel-Like Factor Transcriptional Activity via Its Interaction with the SWI-SNF Complex." Molecular and Cellular Biology 21, no. 7 (April 1, 2001): 2413–22. http://dx.doi.org/10.1128/mcb.21.7.2413-2422.2001.

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ABSTRACT Recruitment of modifiers and remodelers to specific DNA sites within chromatin plays a critical role in controlling gene expression. The study of globin gene regulation provides a convergence point within which to address these issues in the context of tissue-specific and developmentally regulated expression. In this regard, erythroid Krüppel-like factor (EKLF) is critical. EKLF is a red cell-specific activator whose presence is crucial for establishment of the correct chromatin structure and high-level transcriptional induction of adult β-globin. We now find, by metabolic labeling-i

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24

Isern, Joan, Stuart T. Fraser, Zhiyong He, Hailan Zhang, and Margaret H. Baron. "Dose-dependent regulation of primitive erythroid maturation and identity by the transcription factor Eklf." Blood 116, no. 19 (November 11, 2010): 3972–80. http://dx.doi.org/10.1182/blood-2010-04-281196.

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Abstract The primitive erythroid (EryP) lineage is the first to differentiate during mammalian embryogenesis. Eklf/Klf1 is a transcriptional regulator that is essential for definitive erythropoiesis in the fetal liver. Dissection of the role(s) of Eklf within the EryP compartment has been confounded by the simultaneous presence of EryP and fetal liver–derived definitive erythroid (EryD) cells in the blood. To address this problem, we have distinguished EryP from their definitive counterparts by crossing Eklf+/− mutant and ϵ-globin::histone H2B-GFP transgenic mice. Eklf-deficient EryP exhibit m

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Funnell, Alister P. W., Christopher A. Maloney, Lucinda J. Thompson, Janelle Keys, Michael Tallack, Andrew C. Perkins, and Merlin Crossley. "Erythroid Krüppel-Like Factor Directly Activates the Basic Krüppel-Like Factor Gene in Erythroid Cells." Molecular and Cellular Biology 27, no. 7 (February 5, 2007): 2777–90. http://dx.doi.org/10.1128/mcb.01658-06.

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ABSTRACT The Sp/Krüppel-like factor (Sp/Klf) family is comprised of around 25 zinc finger transcription factors that recognize CACCC boxes and GC-rich elements. We have investigated basic Krüppel-like factor (Bklf/Klf3) and show that in erythroid tissues its expression is highly dependent on another family member, erythroid Krüppel-like factor (Eklf/Klf1). We observe that Bklf mRNA is significantly reduced in erythroid tissues from Eklf-null murine embryos. We find that Bklf is driven primarily by two promoters, a ubiquitously active GC-rich upstream promoter, 1a, and an erythroid downstrea

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Pilon, Andre M., Jacqueline Beaupre, James J. Bieker, Patrick G. Gallagher, and David M. Bodine. "Multiple Defects of Both Primitive and Definitive Erythrocytes in EKLF-Deficient Mice." Blood 110, no. 11 (November 16, 2007): 1234. http://dx.doi.org/10.1182/blood.v110.11.1234.1234.

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Abstract Erythroid Krüppel-Like Factor (EKLF) is the founding member of the mammalian Krüppel subfamily of transcription factors with 3 C2H2-type zinc fingers. In mice, loss of EKLF is lethal at day 14 of gestation (dE14), due to severe anemia. To study the physiological properties of the mixed population of circulating primitive and definitive erythrocytes in dE13.5 mice, we developed an osmotic fragility assay that compares the relative amount of embryonic (primitive) and adult (definitive) hemoglobin in the supernatant and pellet of cells exposed to increasing concentrations of NaCl. We f

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Singleton, Belinda K., Victoria SS Fairweather, Winnie Lau, Stephen F. Parsons, Nicholas M. Burton, Jan Frayne, R. Leo Brady, and David J. Anstee. "A Novel EKLF Mutation in a Patient with Dyserythropoietic Anemia: The First Association of EKLF with Disease in Man." Blood 114, no. 22 (November 20, 2009): 162. http://dx.doi.org/10.1182/blood.v114.22.162.162.

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Abstract Abstract 162 We describe a single-point mutation in the transcription factor EKLF associated with dyserythropoietic anemia. The female Danish patient was extensively studied in the early 1990's (Wickramasinghe et al. Br J Haem 1991,79:322; Tang et al. Blood 1993,81:1636; Parsons et al. Blood 1994,83:860; Agre et al. J Clin Invest 1994,94:1050). The patient was severely anemic at birth and required repeated transfusions during childhood. Notable features included persistent expression of epsilon and zeta embryonic globins, an HbF level of 40%, novel intra-erythroblastic and intra-eryth

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28

Zhu, Jianqiong, Kyung Chin, Wulin Aerbajinai, Chutima Kumkhaek, Hongzhen Li, Matthew M. Hsieh, Courtney D. Fitzhugh, and Griffin P. Rodgers. "A Novel Recombinant Eklf-GATA1 Fusion Protein Reduces Sickling of Erythrocytes Cultured from CD34+ Cells with Sickle Cell Disease." Blood 128, no. 22 (December 2, 2016): 3506. http://dx.doi.org/10.1182/blood.v128.22.3506.3506.

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Abstract Current gene therapy approaches for treatment of hemoglobinopathies involve viral transduction of hematopoietic stem cells with antisickling globin genes. Hemoglobin A2 (HA2, α2δ2), expressed at a low level due to the lack of Eklf binding motif in its promoter region, is fully functional and could be a valid anti-sickling agent in sickle cell disease, as well as a substitute of hemoglobin A in β-thalassemia. We had previously demonstrated that two Eklf-GATA1 fusion proteins could significantly activate δ-globin expression in CD34+ cells from healthy and sickle trait donor's blood. Her

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29

Starck, Joëlle, Nathalie Cohet, Colette Gonnet, Sandrine Sarrazin, Zina Doubeikovskaia, Alexandre Doubeikovski, Alexis Verger, Martine Duterque-Coquillaud, and François Morle. "Functional Cross-Antagonism between Transcription Factors FLI-1 and EKLF." Molecular and Cellular Biology 23, no. 4 (February 15, 2003): 1390–402. http://dx.doi.org/10.1128/mcb.23.4.1390-1402.2003.

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ABSTRACT FLI-1 is an ETS family transcription factor which is overexpressed in Friend erythroleukemia and contributes to the blockage of differentiation of erythroleukemic cells. We show here that FLI-1 represses the transcriptional activity of the β-globin gene promoter in MEL cells and interacts with two of its critical transactivators, GATA-1 and EKLF. Unexpectedly, FLI-1 enhances the stimulating activity of GATA-1 on a GATA-1-responsive promoter but represses that of EKLF on β-globin and an EKLF-responsive artificial promoters. This repressive effect of FLI-1 requires the ETS DNA binding d

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Hung, Chun-Hao, Tung-Liang Lee, Anna Yu-Szu Huang, Kang-Chung Yang, Yu-Chiau Shyu, Shau-Ching Wen, Mu-Jie Lu, Shinsheng Yuan, and Che-Kun James Shen. "A Positive Regulatory Feedback Loop between EKLF/KLF1 and TAL1/SCL Sustaining the Erythropoiesis." International Journal of Molecular Sciences 22, no. 15 (July 27, 2021): 8024. http://dx.doi.org/10.3390/ijms22158024.

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The erythroid Krüppel-like factor EKLF/KLF1 is a hematopoietic transcription factor binding to the CACCC DNA motif and participating in the regulation of erythroid differentiation. With combined use of microarray-based gene expression profiling and the promoter-based ChIP-chip assay of E14.5 fetal liver cells from wild type (WT) and EKLF-knockout (Eklf−/−) mouse embryos, we identified the pathways and direct target genes activated or repressed by EKLF. This genome-wide study together with the molecular/cellular analysis of the mouse erythroleukemic cells (MEL) indicate that among the downstrea

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Pilon, Andre M., Murat O. Arcasoy, Serena E. Vayda, Holly K. Dressman, James J. Bieker, David M. Bodine, and Patrick G. Gallagher. "Defects in E2F1/2 Expression Are Associated with Abnormalities in Cell Cycle and Differentiation in EKLF-Deficient Erythroid Cells." Blood 108, no. 11 (November 16, 2006): 84. http://dx.doi.org/10.1182/blood.v108.11.84.84.

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Abstract Mice deficient in the erythroid transcription factor EKLF die ~dE14 from severe anemia, attributed to decreased β-globin expression. Recent reports using microarray analyses indicate that expression of numerous genes is perturbed in erythroid cells lacking EKLF. We performed flow cytometry of WT dE14 fetal liver (FL) cells with TER119 and CD71 and identified 5 previously described populations: R1+R2 composed of BFU-E and CFU-E, respectively, and R3+R4+R5 composed of more mature erythroblasts. The same analysis of dE14 EKLF-deficient FL cells showed R3+R4+R5 were absent, indicating a b

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Zhu, Jianqiong, Hongzhen Li, Wulin Aerbajinai, Chutima Kumkhaek, Kyung Chin, and Griffin Rodgers. "A Novel Recombinant Eklf-GATA1 Fusion Protein Reduces Sickling of Cultured Mouse Erythrocytes." Blood 132, Supplement 1 (November 29, 2018): 3479. http://dx.doi.org/10.1182/blood-2018-99-115209.

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Abstract β-hemoglobinopathies are inherited disorders caused by mutations/deletions in the β-globin chain that lead to structurally defective β-globin chains or reduced (or absent) β-globin chain production. These diseases affect multiple organs and are associated with considerable morbidity and mortality, representing a major public health challenge. Current gene therapy approaches for the treatment of hemoglobinopathies involve viral transduction of hematopoietic stem cells with antisickling globin genes. Hemoglobin A2 (HA2, α2δ2), expressed at a low level due to the lack of Eklf binding mot

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Jansen, Valerie M., Tatiana Abramova, Eun-Hee Shim, Shaji Ramachandran, Aurelie Desgardin, Vishwas Parekh, Stephen Jane, and John M. Cunningham. "Altered Erythroid and Megakaryocytic Differentiation in Mice Expressing a Unique Chromatin Remodeling Domain of Erythroid Krüppel-Like Factor (EKLF)." Blood 112, no. 11 (November 16, 2008): 132. http://dx.doi.org/10.1182/blood.v112.11.132.132.

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Abstract The zinc finger-encoding transacting factor EKLF binds key regulatory elements of many erythroid-specific genes, and is essential for definitive erythropoiesis. Mice lacking this factor (EKLF−/−) die of anemia by E15.5 of gestation, failing to activate β-globin gene transcription, and demonstrating a block in the erythroid differentiation program at the primitive erythroblast stage. In contrast, megakaryocytic progenitors are amplified in EKLFnull embryos, with increased Fli-1 gene expression (a marker of early megakaryocytic differentiation), consistent with the idea that EKLF modula

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Bieker, J. J., and C. M. Southwood. "The erythroid Krüppel-like factor transactivation domain is a critical component for cell-specific inducibility of a beta-globin promoter." Molecular and Cellular Biology 15, no. 2 (February 1995): 852–60. http://dx.doi.org/10.1128/mcb.15.2.852.

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Erythroid Krüppel-like factor (EKLF) is an erythroid cell-specific DNA-binding protein that activates transcription from the beta-globin CACCC element, a functionally important and evolutionarily conserved component of globin as well as other erythroid cell-specific promoters and enhancers. We have attempted to elucidate the molecular role of EKLF in erythrocyte-specific transcriptional activation. First, in vivo and in vitro analyses have been used to demonstrate that the level of activation by EKLF is dependent on the orientation and number of CACCC elements, that EKLF contains separable act

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Singleton, Belinda K., Winnie Lau, Victoria S. S. Fairweather, Nicholas M. Burton, Marieangela C. Wilson, Steve F. Parsons, Ben M. Richardson, et al. "Mutations in the second zinc finger of human EKLF reduce promoter affinity but give rise to benign and disease phenotypes." Blood 118, no. 11 (September 15, 2011): 3137–45. http://dx.doi.org/10.1182/blood-2011-04-349985.

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Abstract Mutations in the human erythroid Krüppel-like factor (EKLF) can lead to either anemia or the benign InLu phenotype. To elucidate the relationship between these mutations and the differing phenotypes, we prepared recombinant forms of wild-type and 5 mutant EKLF proteins and quantitated their binding affinity to a range of EKLF-regulated genes. Missense mutants (R328H, R328L, and R331G) from persons with InLu phenotype did not bind DNA. Hence, as with the heterozygous loss of function nonsense (L127X, S270X, and K292X) and frameshift (P190Lfs and R319Efs) EKLF mutations, monoallelic los

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Shyu, Yu-Chiau, Tung-Liang Lee, Shau-Ching Wen, Hsin Chen, Wei-Yuan Hsiao, Xin Chen, JauLang Hwang та Che-Kun James Shen. "Subcellular Transport of EKLF and Switch-On of Murine Adult βmaj Globin Gene Transcription". Molecular and Cellular Biology 27, № 6 (22 січня 2007): 2309–23. http://dx.doi.org/10.1128/mcb.01875-06.

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ABSTRACT Erythroid Krüppel-like factor (EKLF) is an essential transcription factor for mammalian β-like globin gene switching, and it specifically activates transcription of the adult β globin gene through binding of its zinc fingers to the promoter. It has been a puzzle that in the mouse, despite its expression throughout the erythroid development, EKLF activates the adult βmaj globin promoter only in erythroid cells beyond the stage of embryonic day 10.5 (E10.5) but not before. We show here that expression of the mouse βmaj globin gene in the aorta-gonad-mesonephros region of E10.5 embryos

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Zhu, Jianqiong, Kyung Chin, Wulin Aerbajinai, Cecelia Trainor, Peter Gao, and Griffin P. Rodgers. "Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and gamma-globin expression in erythroid cells." Blood 117, no. 11 (March 17, 2011): 3045–52. http://dx.doi.org/10.1182/blood-2010-07-294751.

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Abstract The β-hemoglobinopathies sickle cell disease and β-thalassemia are among the most common human genetic disorders worldwide. Hemoglobin A2 (HbA2, α2δ2) and fetal hemoglobin (HbF, α2γ2) both inhibit the polymerization of hemoglobin S, which results in erythrocyte sickling. Expression of erythroid Kruppel-like factor (EKLF) and GATA1 is critical for transitioning hemoglobin from HbF to hemoglobin A (HbA, α2β2) and HbA2. The lower levels of δ-globin expression compared with β-globin expression seen in adulthood are likely due to the absence of an EKLF-binding motif in the δ-globin proxima

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Chen, Xiaoyong, and James J. Bieker. "Unanticipated Repression Function Linked to Erythroid Krüppel-Like Factor." Molecular and Cellular Biology 21, no. 9 (May 1, 2001): 3118–25. http://dx.doi.org/10.1128/mcb.21.9.3118-3125.2001.

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ABSTRACT The erythroid cell-specific transcription factor erythroid Krüppel-like factor (EKLF) is an important activator of β-globin gene expression. It achieves this by binding to the CACCC element at the β-globin promoter via its zinc finger domain. The coactivators CBP and P300 interact with, acetylate, and enhance its activity, helping to explain its role as a transcription activator. Here we show that EKLF can also interact with the corepressors mSin3A and HDAC1 (histone deacetylase 1) through its zinc finger domain. When linked to a GAL4 DNA binding domain, full-length EKLF or its zinc

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Ma, Wen-Bing, Xiao-Han Wang, Chang-Yan Li, Huan-Huan Tian, Jie Zhang, Jun-Jie Bi, Guang-Ming Ren, et al. "GPS2 promotes erythroid differentiation by control of the stability of EKLF protein." Blood 135, no. 25 (June 18, 2020): 2302–15. http://dx.doi.org/10.1182/blood.2019003867.

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Abstract Erythropoiesis is a complex multistage process that involves differentiation of early erythroid progenitors to enucleated mature red blood cells, in which lineage-specific transcription factors play essential roles. Erythroid Krüppel-like factor (EKLF/KLF1) is a pleiotropic erythroid transcription factor that is required for the proper maturation of the erythroid cells, whose expression and activation are tightly controlled in a temporal and differentiation stage-specific manner. Here, we uncover a novel role of G-protein pathway suppressor 2 (GPS2), a subunit of the nuclear receptor

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Zhu, Jianqiongz, Kyung Chin, Wulin Aerbajinai, Cecelia D. Trainor, Gao Perter та Griffin P. Rodgers. "Recombinant Erythroid Kruppel-Like Factor Fused to GATA1 up-Regulates δ-Globin Expression In Erythroid Cells." Blood 116, № 21 (19 листопада 2010): 3752. http://dx.doi.org/10.1182/blood.v116.21.3752.3752.

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Abstract Abstract 3752 The β-hemoglobinopathies sickle cell disease and β-thalassemia are among the most common human genetic disorders worldwide. Hemoglobin A2 (HbA2, α2δ2) and fetal hemoglobin (HbF, a2γ2) both inhibit the polymerization of hemoglobin S that results in erythrocyte sickling. Expression of erythroid Kruppel-like factor (EKLF) and GATA1 is critical for transitioning hemoglobin from HbF to hemoglobin A (HbA, α2β2) and HbA2. The lower levels of δ-globin expression compared with β-globin expression seen in adulthood are likely due to the absence of an EKLF-binding motif in the δ-gl

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Pilon, Andre M., Dewang Zhou, Mitchell J. Weiss, Timothy M. Townes, David M. Bodine, and Patrick G. Gallagher. "The Human Alpha Hemoglobin Stabilizing Protein (AHSP) Gene Locus in EKLF-Deficient Erythroid Cells." Blood 106, no. 11 (November 16, 2005): 1740. http://dx.doi.org/10.1182/blood.v106.11.1740.1740.

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Abstract AHSP is an erythroid-specific protein that complexes with free α-hemoglobin, protecting it from precipitation. AHSP has been proposed as a modifier gene in β thalassemia and as a candidate gene for unexplained Heinz body anemias, thus understanding its regulation may lead to novel therapies for these disorders. Identified as an erythroid-specific, GATA-1 inducible gene, decreased AHSP mRNA has been found in the fetal livers of mice deficient in the erythroid transcription factor EKLF by both microarray and RNA subtraction analysis. In fetal livers from d13.5 EKLF-deficient mice, AHSP/

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Siatecka, Miroslawa, Li Xue, and James J. Bieker. "Sumoylation of EKLF Promotes Transcriptional Repression and Is Involved in Inhibition of Megakaryopoiesis." Molecular and Cellular Biology 27, no. 24 (October 15, 2007): 8547–60. http://dx.doi.org/10.1128/mcb.00589-07.

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ABSTRACT Erythroid Krüppel-like factor (EKLF [KLF1]) is a transcriptional regulator that plays a critical role within a specific subset of hematopoietic cells, particularly in the erythroid lineage and its immediate precursor, the megakaryocyte-erythroid progenitor (MEP). We find that EKLF is posttranslationally modified by sumoylation at a single site near its amino terminus and that PIAS1 plays a critical role in this process. Mutation of this site has little effect on EKLF's ability to function as a transcriptional activator; however, it has a dramatic effect on its repressive abilities. T

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Gallagher, Patrick G., Murat O. Arcasoy, Serena E. Vayda, Holly K. Dressman, James J. Bieker, and David M. Bodine. "A Differentiation Block in Erythroid Cells Lacking Erythroid Krupple-Like Factor (EKLF)." Blood 106, no. 11 (November 16, 2005): 526. http://dx.doi.org/10.1182/blood.v106.11.526.526.

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Abstract Mice deficient in the erythroid specific zinc-finger transcription factor EKLF die ~d14-15 of gestation of severe anemia, attributed to decreased expression of β-globin. The morphology of fetal-liver derived erythroid cells in EKLF-deficient mice does not mimic that seen in thalassemia, but instead shows hemolysis with uniform, nucleated erythroid progenitor cells. This has led to the hypothesis that a block in erythroid differentiation contributes to the anemia in EKLF-deficient mice. To address this, we performed microarray analyses with Affymetrix GeneChip Mouse Genome 430 2.0 arra

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Guy, Louis-Georges, Qi Mei, Andrew C. Perkins, Stuart H. Orkin та Lee Wall. "Erythroid Krüppel-Like Factor Is Essential for β-Globin Gene Expression Even in Absence of Gene Competition, But Is Not Sufficient to Induce the Switch From γ-Globin to β-Globin Gene Expression". Blood 91, № 7 (1 квітня 1998): 2259–63. http://dx.doi.org/10.1182/blood.v91.7.2259.

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Abstract Different genes in the β-like globin locus are expressed at specific times during development. This is controlled, in part, by competition between the genes for activation by the locus control region. In mice, gene inactivation of the erythroid Krüppel-like factor (EKLF) transcription factor results in a lethal anemia due to a specific and substantial decrease in expression of the fetal/adult-stage–specific β-globin gene. In transgenic mice carrying the complete human β-globin locus, EKLF ablation not only impairs human β-globin–gene expression but also results in increased expressio

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Guy, Louis-Georges, Qi Mei, Andrew C. Perkins, Stuart H. Orkin та Lee Wall. "Erythroid Krüppel-Like Factor Is Essential for β-Globin Gene Expression Even in Absence of Gene Competition, But Is Not Sufficient to Induce the Switch From γ-Globin to β-Globin Gene Expression". Blood 91, № 7 (1 квітня 1998): 2259–63. http://dx.doi.org/10.1182/blood.v91.7.2259.2259_2259_2263.

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Different genes in the β-like globin locus are expressed at specific times during development. This is controlled, in part, by competition between the genes for activation by the locus control region. In mice, gene inactivation of the erythroid Krüppel-like factor (EKLF) transcription factor results in a lethal anemia due to a specific and substantial decrease in expression of the fetal/adult-stage–specific β-globin gene. In transgenic mice carrying the complete human β-globin locus, EKLF ablation not only impairs human β-globin–gene expression but also results in increased expression of the

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Singleton, Belinda K., Nicholas M. Burton, Carole Green, R. Leo Brady, and David J. Anstee. "Mutations in EKLF/KLF1 form the molecular basis of the rare blood group In(Lu) phenotype." Blood 112, no. 5 (September 1, 2008): 2081–88. http://dx.doi.org/10.1182/blood-2008-03-145672.

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Abstract Comparison of normal erythroblasts and erythroblasts from persons with the rare In(Lu) type of Lu(a-b-) blood group phenotype showed increased transcription levels for 314 genes and reduced levels for 354 genes in In(Lu) cells. Many erythroid-specific genes (including ALAS2, SLC4A1) had reduced transcript levels, suggesting the phenotype resulted from a transcription factor abnormality. A search for mutations in erythroid transcription factors showed mutations in the promoter or coding sequence of EKLF in 21 of 24 persons with the In(Lu) phenotype. In all cases the mutant EKLF allele

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Varricchio, Lilian, Carmela Dell'Aversana, Angela Nebbioso, Giovanni Migliaccio, Lucia Altucci, James J. Bieker, and Anna Rita F. Migliaccio. "Identification of a New Functional HDAC Complex Composed by HDAC5, GATA1 and EKLF in Human Erythroid Cells." Blood 120, no. 21 (November 16, 2012): 979. http://dx.doi.org/10.1182/blood.v120.21.979.979.

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Abstract Abstract 979 Histone deacetylation, the reaction that maintains chromatin in a condensed configuration preventing gene expression, is catalyzed by the histone deacetylase (HDAC) superfamily. The human HDAC family includes 18 different isoforms classified on the basis of their sequence homology to HDACs from Saccharomyces Cerevisiae into class I (HDAC1, −2, −3, and −8), IIa (HDAC4, −5, −7, and −9), IIb (HDAC6 and −10) and IV (HDAC11). Class I HDACs bind the DNA directly while class IIa HDACs shuffles other proteins between nucleus and cytoplasm. While the role of individual class I HDA

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Pilon, Andre M., Clara Wong, Lisa J. Garrett-Beal, Mitchell Weiss, Patrick G. Gallagher, and David M. Bodine. "Chromatin Remodeling of the Mouse AHSP Gene Requires EKLF." Blood 104, no. 11 (November 16, 2004): 375. http://dx.doi.org/10.1182/blood.v104.11.375.375.

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Abstract Alpha-Hemoglobin Stabilizing Protein (AHSP) is an erythroid-specific protein that binds to α-globin, preventing precipitation of α-hemoglobin tetramers. Our interest has focused on how the AHSP gene is specifically expressed in erythroid cells, and we have investigated the roles of cis acting DNA sequences, the transcription factor EKLF and chromatin structure on AHSP gene expression. We have previously shown that the AHSP gene has a single mRNA initiation site followed by a non-coding exon. Putative promoter sequences from −904, −479 or −170 were active in luciferase reporter assays

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Neuwirtova, Radana, Ota Fuchs, Dana Provaznikova, Jaroslav Cermak, Magda Siskova, Anna Jonasova, and Kyra Michalova. "Fli-1 and EKLF Gene Expression in Patients with MDS 5q- Syndrome." Blood 114, no. 22 (November 20, 2009): 2788. http://dx.doi.org/10.1182/blood.v114.22.2788.2788.

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Abstract Abstract 2788 Poster Board II-764 Introduction. Patients with MDS-5q- syndrome have macrocytic anemia often with hypoplastic erythropoiesis and on the contrary thrombocythemia with effective though dysplastic megakaryopoiesis. Megakaryocytes and erythroid cells are thought to share a common progenitor MEP (T.P.McDonald et al., Exp. Hematology 1993). There are two key transcription factors which together with other transcription factors and relevant cytokines and receptors determine the hemopoietic differentiation of the common stem cell: erythroid Krüppel-like factor (EKLF) for eryth

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50

Siatecka, Miroslawa, Felix Lohmann, Sujin Bao, and James J. Bieker. "EKLF Directly Activates the p21WAF1/CIP1 Gene by Proximal Promoter and Novel Intronic Regulatory Regions during Erythroid Differentiation." Molecular and Cellular Biology 30, no. 11 (April 5, 2010): 2811–22. http://dx.doi.org/10.1128/mcb.01016-09.

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ABSTRACT The switch from proliferation to differentiation during the terminal stages of erythropoiesis is a tightly controlled process that relies in part on transcription factor-mediated activation of cell cycle components. EKLF is a key transcription factor that is necessary for the initial establishment of the red cell phenotype. Here, we find that EKLF also plays a role during the subsequent differentiation process, as it induces p21WAF1/CIP1 expression independent of p53 to regulate the changes in the cell cycle underlying erythroid maturation. EKLF activates p21 not only by directly bind

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